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Target Concepts:
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Query: UMLS:C0032463 (
polycythemia vera
)
3,374
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Incorporation of [32P]-orthophosphate into plasma phospholipids was investigated in 11 patients with
polycythemia vera
. The specific activity of phospholipid radioactive precursors (
TCA
-extract) was maximal 1 hour after the delivery of radioactive phosphorus and dropped to less than 20 per cent of maximal value after 24 hours. The peak of total phospholipid specific activity was observed 48 hours after the administration of [32P]-orthophosphate in 10 patients, and after 24 hours in one, and decreases regularly afterward. The half-life of the lipid-bound phosphorus in the plasma of investigated patients, determined during the decrease of their specific activity was 252+/-60 hours. Concentration of total plasma phospholipids and the pattern of individual phospholipid found in patients with
polycythemia vera
were similar to those reported for normal individuals. The rate of incorporation of the labeled phosphorus into phosphatidylethanolamine and phosphatidic acid was much more rapid than into lysophosphatidylcholine, sphingomyelin, or phosphatidylcholine.
...
PMID:Incorporation of [32P]-orthophosphate into total and individual plasma phospholipids in patients with polycythemia vera. 115 Nov 51
The autonomic regulation of hepatic metabolism offers a novel target for the treatment of non-alcoholic fatty liver disease (NAFLD). However, the molecular characteristics of neurons that regulate the brain-liver axis remain unclear. Since mice lacking neuronal lipoprotein lipase (LPL) develop perturbations in neuronal lipid-sensing and systemic energy balance, we reasoned that LPL might be a component of pre-autonomic neurons involved in the regulation of hepatic metabolism. Here, we show that, despite obesity, mice with reduced neuronal LPL (NEXCreLPL
flox
(LPL KD)) show improved glucose tolerance and reduced hepatic lipid accumulation with aging compared to wilt type (WT) controls (LPL
flox
). To determine the effect of LPL deficiency on neuronal physiology, liver-related neurons were identified in the paraventricular nucleus (PVN) of the hypothalamus using the transsynaptic retrograde tracer
PRV
-152. Patch-clamp studies revealed reduced inhibitory post-synaptic currents in liver-related neurons of LPL KD mice. Fluorescence lifetime imaging microscopy (FLIM) was used to visualize metabolic changes in LPL-depleted neurons. Quantification of free vs. bound nicotinamide adenine dinucleotide (NADH) and flavin adenine dinucleotide (FAD) revealed increased glucose utilization and
TCA
cycle flux in LPL-depleted neurons compared to controls. Global metabolomics from hypothalamic cell lines either deficient in or over-expressing LPL recapitulated these findings. Our data suggest that LPL is a novel feature of liver-related preautonomic neurons in the PVN. Moreover, LPL loss is sufficient to cause changes in neuronal substrate utilization and function, which may precede changes in hepatic metabolism.
...
PMID:Neuronal Lipoprotein Lipase Deficiency Alters Neuronal Function and Hepatic Metabolism. 3299 80
